Our previous investigation showed that subjects receiving finger temperature feedback could increase finger temperature, without relaxation or decreased stress, and maintain this effect one year later. In the proposed investigations, we will first determine the long-term duration of these effects and the possible influence of booster training on them. Since temperature feedback appears to operate in the absence of relaxation, we will next attempt to determine its physiological mechanism using pharmacological probes. A beta-adrenergic vasodilating mechanism has recently been discovered in the finger; we propose to determine if this is involved in the mechanism of finger temperature feedback in Raynaud's disease patients and normal subjects. Since we have also shown that Raynaud's disease patients have chronically low levels of digital blood flow without increased SNS activity, we will also compare alpha and beta receptor sensitivity in the digital blood vessels of these patients and matched controls. Lastly, since temperature feedback appears promising in the treatment of Raynaud's phenomenon in scleroderma, we will attempt to replicate our previous findings in a new group of patients with Raynaud's phenomenon secondary to mixed connective tissue disease (MCTD).